The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Arid3a  -  AT rich interactive domain 3A (BRIGHT-like)

Mus musculus

Synonyms: ARID domain-containing protein 3A, AT-rich interactive domain-containing protein 3A, B-cell regulator of IgH transcription, Bright, Dead ringer-like protein 1, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

High impact information on Arid3a

  • This B-cell specific protein, termed Bright (B cell regulator of IgH transcription), is found in both soluble and matrix insoluble nuclear fractions [1].
  • Our study also revealed that recombinant marine (rm)IL-2 and rmIL-7 reciprocally induced high expressions of IL-7R and IL-2R, respectively, on gamma delta (Dim) T cells but not on gamma delta (Bright) cells [2].
  • Our earlier reports demonstrated that Bright coimmunoprecipitates with Bruton's tyrosine kinase (Btk) and that these proteins associate in a DNA-binding complex in primary B cells [3].
  • In order to determine if Btk is important for Bright function, a transcription activation assay was established and analyzed using real-time PCR technology [3].
  • Cux/CDP antagonizes the effects of the Bright transcription activator at both the DNA binding and functional levels [4].

Biological context of Arid3a

  • Immunoglobulin gene transcription was enhanced when Bright and Btk were coexpressed [3].
  • Bright activation results in up-regulation of mu transcription; however, it is not clear whether Bright function is critical for normal B cell development [5].
  • We expected to find Bright expression in a subset of mature spleen cells, but also observed Bright in a subset of normal B lymphocytic progenitors in both adult bone marrow (BM) and in fetal liver as early as day 12 of gestation [6].
  • In this study, we have used transgenic animals to test the functional importance of a 5' portion of the VH1 promoter which is known to contain a matrix attachment region as well as binding sites for the negative regulator NF-microNR and Bright, a protein complex which is induced upon stimulation of B cells with IL-5 and antigen [7].

Anatomical context of Arid3a


Regulatory relationships of Arid3a

  • Thus, the ability of Bright to enhance immunoglobulin transcription critically requires functional Btk [3].

Other interactions of Arid3a

  • B cells from immunodeficient mice with a mutation in Btk failed to produce stable Bright DNA-binding complexes [3].

Analytical, diagnostic and therapeutic context of Arid3a


  1. The immunoglobulin heavy-chain matrix-associating regions are bound by Bright: a B cell-specific trans-activator that describes a new DNA-binding protein family. Herrscher, R.F., Kaplan, M.H., Lelsz, D.L., Das, C., Scheuermann, R., Tucker, P.W. Genes Dev. (1995) [Pubmed]
  2. Interleukin 2 (IL-2) and interleukin 7 (IL-7) reciprocally induce IL-7 and IL-2 receptors on gamma delta T-cell receptor-positive intraepithelial lymphocytes. Fujihashi, K., Kawabata, S., Hiroi, T., Yamamoto, M., McGhee, J.R., Nishikawa, S., Kiyono, H. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  3. Bruton's tyrosine kinase regulates immunoglobulin promoter activation in association with the transcription factor Bright. Rajaiya, J., Hatfield, M., Nixon, J.C., Rawlings, D.J., Webb, C.F. Mol. Cell. Biol. (2005) [Pubmed]
  4. Cux/CDP homeoprotein is a component of NF-muNR and represses the immunoglobulin heavy chain intronic enhancer by antagonizing the bright transcription activator. Wang, Z., Goldstein, A., Zong, R.T., Lin, D., Neufeld, E.J., Scheuermann, R.H., Tucker, P.W. Mol. Cell. Biol. (1999) [Pubmed]
  5. Mutations in the DNA-binding domain of the transcription factor Bright act as dominant negative proteins and interfere with immunoglobulin transactivation. Nixon, J.C., Rajaiya, J., Webb, C.F. J. Biol. Chem. (2004) [Pubmed]
  6. Expression of bright at two distinct stages of B lymphocyte development. Webb, C.F., Smith, E.A., Medina, K.L., Buchanan, K.L., Smithson, G., Dou, S. J. Immunol. (1998) [Pubmed]
  7. A 125 bp region of the Ig VH1 promoter is sufficient to confer lymphocyte-specific expression in transgenic mice. Avitahl, N., Calame, K. Int. Immunol. (1996) [Pubmed]
  8. The transcription factor Bright associates with Bruton's tyrosine kinase, the defective protein in immunodeficiency disease. Webb, C.F., Yamashita, Y., Ayers, N., Evetts, S., Paulin, Y., Conley, M.E., Smith, E.A. J. Immunol. (2000) [Pubmed]
WikiGenes - Universities